The cause of a spinal cord injury may be either traumatic or non-traumatic. Spinal cord injuries of the former type are caused by, for example, traffic accidents, sporting accidents, or workplace accidents, whereas those of the latter group are caused by, for example, inflammation, bleeding, tumors, or deformed vertebrae. Most spinal cord injuries are traumatic. Symptoms of spinal injuries include motor function disorders and sensory disturbances.
Spinal injuries are treated primarily by symptomatic therapy by use of a neuroprotective agent or a brain metabolism enhancer, and no therapy can restore neurons lost by spinal cord injury.
Meanwhile, we have seen progress in neuroscience related to spinal cord injury. Specifically, studies have clarified that in adult spinal injuries, despite the presence of endogenous neural stem cells in the spinal cord, neogenesis of neurons or oligodendrocytes does not occur, permitting differentiation and proliferation of astrocytes and resulting in formation of glial scar, which prevents axonal regeneration.
A single case of successful neural regeneration within damaged spinal cord heretofore reported is a rat spinal cord injury case, where transplantation of a fetal rat spinal cord was performed and found effective (Diener P S and Bregman B S, J. Neurosci., 18(2): 779-793(1998), Diener P S and Bregman B S, J. Neurosci., 18(2), 763-778(1998)).
When application to humans of this single case of success is pursued, large amounts of human fetal spinal cords required for transplantation procedure must be secured. However, procurement of such massive human fetal spinal cords is not realistic and is actually not applicable in practice.
Accordingly, an object of the present invention is to create a spinal cord injury model in an animal which is closer to the human, to thereby provide a method for treating spinal injuries which can be applied to humans.